Upper Respiratory Diseases of Horses Flashcards
1
Q
Etiology of Strangles
A
Streptococcus equi equi
highly host adapted
2
Q
Epizootiology of Strangles
A
Transmission:
- direct contact
- indirect: contaminated buckets, feed, pasture…
Outbreaks occur where large groups of animals are brought together
- morbidity: 30-100%
- mortality: <10%
3
Q
Pathogenesis of Strangles
A
ingestion or inhalation –> attachment to tonsils and translocation below mucosa in the lymphatics –> multiplication in local lymph nodes –> lymph node abscessation –> dissemination may occur (hematogenous or via lymphatics)
4
Q
Clinical signs of Strangles
A
- incubation period 3-14 days
- fever, depression
- bilateral nasal discharge (serous then purulent)
- lymphadenopathy (submandibular and retropharyngeal)
- respiratory distress
- abscesses may occur anywhere on the body
5
Q
Chronic carriers of Strangles
A
- most horses stop shedding 3-6 weeks after resolution of clinical signs
- some horses will become chronic asymptomatic carriers
- guttural pouch is the site of carriage in >80% of horses
- shedding may last for several months, even years
6
Q
Diagnosis of Strangles
A
- abscessed lymph nodes are sufficient for a presumptive dx
- culture or PCR amplification
- abscess aspirate
- nasal or pharyngeal swab
- nasal flush (3x negative)***
- guttural pouch flush (1x negative)
7
Q
Treatment of Strangles
A
- early (before abscessation): +/- penicillin
- horses with lymph node abscessation
- promote maturation and drainage of abscessed lymph nodes
- no abx unless pneumonia or respiratory distress
- supportive therapy
- horses exposed to S. equi equi: penicillin
8
Q
Strangles Complications
A
- pneumonia
- guttural pouch empyema and/or chondroids
- bastard strangles (metastatic)
- myocarditis, endocarditis (rare)
- glomerulonephritis
- purpura hemorrhagica
9
Q
purpura hemorrhagica (strangles)
A
- acute necrotizing immune-mediated vasculitis
- 2-4 weeks after outbreak
- pathophysiology:
- immune complexes -> deposition in blood vessels -> complement activation and mediator release -> vessel wall necrosis
10
Q
Purpura hemorrhagica clinical signs
A
- warm and painful edema of the limb, ventral abdomen and face
- may progress to skin necrosis and sloughing
- petechial hemorrhage
- +/- fever
- stiffness, reluctance to move
11
Q
Diagnosis of purpura hemorrhagica
A
- history and clinical signs
- skin biopsy
12
Q
Treatment of purpura hemorrhagica
A
- systemic antimicrobials
- penicillin +/- gram-negative coverage
- corticosteroids
- supportive therapy (NSAIDs, hydrotherapy, bandages)
13
Q
Vaccination for Strangles
A
- intramuscular
- M protein extracts
- intranasal (Pinnacle IN)
14
Q
Guttural pouch anatomy
A
- diverticulum of the Eustachian tubes
- medial compartment:
- internal carotid
- cranial nerves IX, X, XI, XII
- cranial cervical ganglion
- lateral compartment
- external carotid artery
- maxillary artery
- cranial nerve VII
- medial compartment:
15
Q
Guttural pouch empyema
A
accumulation of exudate in the guttural pouches
- unilateral or bilateral
- sometimes the exudate may solidify (chondroids)
16
Q
Clinical signs of guttural pouch empyema
A
- nasal discharge when head down (greater on the affected side)
- rarely dysphagia
- not usually malodorous
17
Q
Diagnosis of GP empyema
A
- endoscopy
- radiographs: fluid line or chondroids
- culture:
- Streptococcus equi zooepidemicus
- Streptococcus equi equi
18
Q
Treatment of GP empyema
A
- lavage with large volumes of saline
- antibiotics
- sx to remove chondroids
19
Q
Guttural pouch mycosis
A
fungal infections often over a major blood vessel (usually internal carotid)
20
Q
Clinical signs of GP mycosis
A
- epistaxis
- dysphagia
- other (Horner’s syndrome, laryngeal hemiplegia…)
21
Q
Diagnosis of GP mycosis
A
- endoscopy
- culture
- Emericella nidulans
- Aspergillus spp. or other fungi
22
Q
Treatment of GP mycosis
A
- surgical: proximal and distal occlusion of the affected artery
- medical: not recommended if severe epistaxis
23
Q
Guttural pouch tympany
A
- distension of one or both guttural pouches with air (horses less than 1 year of age)
- clinical signs:
- external swelling in parotid area
- dyspnea if severe
- rarely dysphagia
- diagnosis:
- clinical signs
- treatment:
- surgical
24
Q
Sinusitis
A
- primary
- maxillary sinus is most commonly affected
- S. equi zooepidemicus is commonly involved
- secondary
- tooth root abscess
25
Clinical signs of sinusitis
* nasal discharge (unilateral)
* ozena (halitosis)
* ocular discharge
* facial sensitivity/deformity
26
Diagnosis of sinusitis
* percussion
* radiographs
* endoscopy
* oral exam
* CT
27
Treatment of sinusitis
* primary
* systemic antibiotics
* sinus flush
* secondary
* systemic antibiotics
* tooth extraction
* tooth repulsion through a maxillary sinus flap
28
Viral respiratory diseases
* influenza
* Herpes virus (rhinopneumonitis)
* clinical signs: fever, cough, and nasal discharge
* diagnosis:
* virus isolation
* \*\*\*PCR amplification
* serology
* antigen detection
29
Equine Influenza
* most common cause of severe epidemics of upper respiratory disease in horses
* orthomyxovirus with a RNA genome
* only influenza type A affects horses
* antigenic determinants
* hemagglutinin (HA)
* neuraminidase (NA)
30
Pathogenesis of Equine Influenza
* only two types have been recognized in horses
* A/equine 1 (H7N7)
* A/equine 2 (H3N8) major subtype in horses
* antigenic drift
* incubation 1-3 days
* infect mainly 1-3 year old horses in training
* infection -\> adhesion to respiratory epithelium -\> desquamation of ciliated cells -\> decreased mucociliary clearance
* low mortality, high morbidity (up to 100%)
31
Clinical signs of Equine Influenza
* acute onset of fever, anorexia and depression
* dry cough
* serous nasal discharge
* submandibular lymph nodes may be slightly enlarged
32
Diagnosis of Equine Influenza
* viral isolation: influenza is difficult to isolate
* **RT-PCR amplification**
* serology: retrospective dx only
* Influenza A Antigen Detection Kit (rapid)
33
Complications of Equine Influenza
* bacterial pneumonia/pleuropneumonia
* myositis, myocarditis
34
Treatment of Equine Influenza
* rest: at least three weeks
* NSAIDs to control fever
* antibiotics if secondary bacterial pneumonia develop
* specific antiviral therapy is usually not warranted
35
Equine Influenza Immunity and Vax
* Immunity: protection lasts 1 year following natural infection
* vax (killed IM): transient systemic IgG response, every 6 months
* vaccination (MLV IN): protects for 6-12 months
* Canary Pox Vector Vaccine: useful in foals of vaccinated dams
36
Equine Herpesvirus
EHV-1: abortion, perinatal dz and death, neurological form (EHM), respiratory dz
EHV-2: immunosuppression?, keratoconjunctivitis
EHV-3: equine coital exanthema
EHV-4: respiratory disease (rhinopneumonitis)
EHV-5: EMPF
37
EHV 1 & EHV 4 Pathogenesis
* most common in young horses (0-3 years)
* responsible for 15-20% of outbreaks of URT dz
* up to 85% of horses carry EHV-1 and/or EHV-4 in a latent state (lymph nodes, trigeminal ganglia)
* acquisition by inhalation or recrudescence of a latent infection
* incubation period 2-10 days
* viremia is common is EHV-1 infections
38
Diagnosis of EHV-1 & 4
* virus isolation or **qPCR amplification**
* nasal swabs
* whole blood (EHV-1)
* serology
39
Vaccination of EHV-1 & 4
* currently available vaccines
* EHV-1, EHV-4 or both
* inactivated or modified live
* label claim: abortion vs respiratory dz
* cross-protection between EHV-1 and EHV-4
40
Foal Pneumonia
* 1-10 months
* leading cause of morbidity and mortality
* inhalation of aerosolized or dust-borne pathogens
* neonates
* bacteremia
* hematogenous spread of bacteria to lungs
41
Clinical signs of Foal Pneumonia
* cough
* nasal discharge (bilateral)
* fever
* increased respiratory rate
* respiratory distress
(any combination)
42
Diagnosis of Foal Pneumonia
* abnormal lung sounds
* hematology
* radiology and u/s
* tracheobronchial aspiration (cytology, gram stain, culture)
* response to tx
43
Etiologic agents of Foal Pneumonia
* *Streptococcus equi zooepidemicus*
* most commonly isolated
* *Rhodococcus equi*
* other bacteria may be primary or occur in association with *S. zooepidemicus* or *R. equi*
* ***Pasteurella, E. coli...*
44
Treatment of Foal Pneumonia
* Abx
* oxygen therapy
* duration of therapy based on: resolution of clinical signs, normal WBC count and fibrinogen concentrations, diagnostic imaging
* minimum of 10 days
45
Prognosis of Foal Pneumonia
most cases make a complete recovery if diagnosed early and treated appropriatedly
46
Pathogenesis of *Rhodococcus equi* Pneumonia
* Gram-positive facultative intracellular pathogen
* can survive and replicate in macrophages
* normal inhabitant in soil
* infection by inhalation
* devastating disease on some farms
47
Clinical manifestations of *R. equi* Pneumonia
* 1 to 6 months of age
* bronchopneumonia
* intestinal manifestations
* nonseptic immune-mediated polysynovitis
* septic arthritis and osteomyelitis
* other manifestations (uveitis, abbscesses)
48
Diagnosis of *R. equi* Pneumonia
* hematology
* radiography and u/s
* tracheobronchial aspiration: **only way to make a definitive diagnosis**
* cytology, gram stain, culture, PCR
49
Treatment of *R. equi* Pneumonia
* macrolide and rifampin
* penetrates caseous material
* achieve good intracellular levels
* long term therapy is require (4-9 weeks)
* macrolides suppress sweating -\> hyperthermia
50
Prognosis of *R. equi* Pneumonia
* survival rate 60-80%
* affected foals are slightly less likely to race
51
Prevention of *R. equi* Pneumonia
* **decreasing size of infective challenge**
* isolate affected foals
* prevent grass destruction and dust formation
* **earlier recognition of the disease**
* **hyperimmune plasma**
* decrease the incidence and severity of the disease
52
Pneumonia
infection involving the lung and parenchyma
53
pleuropneumonia
pneumonia or lung abscess that extends to and invovles the visceral pleura
54
Causes of pleural effusion
* pneumonia
* pleuropneumonia
* hemothorax
* penetrating chest wound
* neoplasia
* hypoproteinemia
* congestive heart failure
55
pathophysiology of pneumonia/pleuropneumonia
* viral infection, toxic gases, stress (transport, race), malnutrition, or general anesthesia
* -\> decreased number and bactericidal activity of alveolar macrophages -\>
* OR excessive number of virulent bacteria -\>
**= pneumonia/pleuropneumonia**
56
Clinical signs of pneumonia/pleuropneumonia
* fever
* anorexia, dperession
* tachypnea, respiratory distress
* cough
* pain on palpation of the thorax
* bilateral nasal discharge (hemorrhagic or purulent)
* fetid breath
* ventral edema
* colic-like signs
* weight loss in chronic cases
57
Infectious agents of pneumonia/pleuropneumonia
* *S. equi zooepidemicus*
* Gram-negative bacteria (*Pasteurella, E. coli...)*
* Anaerobes (*Bacteroides, Eubacterium...)*
58
Diagnosis of pneumonia/pleuropneumonia
* auscultation (absence of or decreased lung sounds ventrally)
* percussion (horizontal line with resonant sounds dorsally and dull sounds ventrally)
* pleurodynia (pleural pain)
* hematology
* u/s
* radiography
* tracheobronchial aspiration (cytology, culture)
* thoracocentesis (cytology, culture)
59
Treatment of pneumonia/pleuropneumonia
* antibiotics
* initial: broad-spectrum abx
* ideal: based on C & S testing
* long term therapy is often required (2-24 wks)
* pleural drainage
* supportive care
* thoracotomy and rib resection (in chronic cases only)
60
Complications of pneumonia/pleuropneumonia
* endotoxemia and thrombophlebitis
* laminitis
* pleural and/or pulmonary abscess formation
* pneumothorax
* pericarditis (rare)
61
Prognosis of pneumonia/pleuropneumonia
depends on severity and duration of clinical signs prior to therapy
62
Exercise-Induced Pulmonary Hemorrhage (EIPH)
* presence of blood in the airways after inense exercise
* pulmonary hemorrhage (caudodorsal lung fields)
* incidence
* 5% of race horses will show epistaxis
* up to 90% of race horses have EIPH
* effects on performance-rule out other causes of exercise intolerance
63
Diagnosis of EIPH
* endoscopy
* cytological examination (TBA or BAL)
* **hemosiderin-laden macrophages-Prussian blue stain**
* thoracic radiography
64
Pathogenesis of EIPH
* failure of pulmonary capillaries during exercise
* pulmonary capillary pressure increased
65
Treatment of EIPH
* Furosemide (loop diuretic)
* pre-race admin to horses with EIPH permitted by most states
* does not prevent hemorrhage but decreases severity
* nasal strips?
66
Heaves
* Equine asthma, RAO
* mature horses (\>3, often \> 7 yo)
* in northern US, stabled horses during winter
* in southern US, more prevalent during summer on pasture
67
Pathogenesis of Heaves
Fungi/Actinomycetes, molds, endotoxins, other allergens, genetic predisposition --\>
* non-specific inflammation
* hypersensitivity
* type I (IgE)
* Type III (IgG or IgM)
**= Inflammatory mediator release** (cytokines, leukotrienes, histamine...)
* -\> bronchiolitis, neutrophilic airway infiltration, excess mucus, bronchoconstriction
68
Clinical signs of Heaves
mild:
* intermittent cough
* exercise intolerance
* abnormal lung sounds
* mild increase in resp rate
severe:
* respiratory distress
* marked abdominal effort during expiration (heave line)
* weight loss
* fever is not present unless the disease is complicated by a secondary bacterial infection
69
Diagnosis of Heaves
* history and physical exam
* increased expiratory effort
* crackles and expiratory wheezes
* lack of fever
* normal WBC count and fibrinogen
* bronchoalveolar lavage
* response to bronchodilators
70
Treatment of Heaves
* environmental changes
* reduce dust and allergen exposure (avoid hay or soak/steam it, move inside, change pasture)
* corticosteroids (**most effective therapy**)
* 2-4 weeks
* inhaled vs systemic
* bronchodilators
* relieve obstruction caused by airway smooth muscle contraction
* do not treat primary problem
* systemic vs inhaled
